InstalabLoading...
InstalabLoading...
Your cells run on a molecule called NAD, and nicotinic acid is one of the raw materials your body uses to make it. NAD is involved in over 400 enzymatic reactions, from turning food into energy to repairing damaged DNA. When nicotinic acid supply drops too low, your ability to build NAD falls with it, and the effects can range from subtle fatigue and metabolic sluggishness to, in severe cases, a life-threatening condition called pellagra.
This test measures circulating nicotinic acid (also called niacin) directly. That makes it a Tier 3, research-level measurement: there are no standardized clinical cutpoints, and the science of interpreting a single blood level is still developing. But for someone tracking their NAD-related biology over time, especially alongside other markers in an NAD profile, nicotinic acid gives you a direct window into whether one of NAD's key precursors is available in your bloodstream.
Nicotinic acid (niacin, vitamin B3) enters your cells and gets converted into NAD through a specific assembly line called the Preiss-Handler pathway. An enzyme in your liver, kidneys, and small intestine grabs nicotinic acid and transforms it step by step into NAD, the molecule your cells depend on for extracting energy from food, repairing DNA breaks, regulating gene activity, and managing calcium signaling.
Your body cannot manufacture nicotinic acid from scratch. You get it from food (meat, fish, legumes, fortified grains) and, interestingly, from your gut bacteria. Your intestinal microbes convert a related B3 form, nicotinamide, into nicotinic acid, which the colon then absorbs. Your liver can also produce small amounts from the amino acid tryptophan, but this conversion is inefficient: roughly 60 mg of tryptophan yields only about 1 mg of usable niacin equivalent.
This distinction matters more than most people realize. Nicotinic acid and nicotinamide (niacinamide) are both called "vitamin B3," and both feed into NAD production. But they are pharmacologically distinct molecules. Only nicotinic acid activates a receptor called GPR109A, which is why only nicotinic acid causes the characteristic flushing reaction and has lipid-modifying properties. Nicotinamide does not do either of those things.
This test measures circulating nicotinic acid specifically, not nicotinamide, not NAD+ itself, and not any of the other members of the NAD family. Results from studies measuring whole-blood NAD+ or tissue NAD+ levels do not directly tell you what your nicotinic acid level means. When reviewing research below, pay attention to which molecule was actually measured. The NAD system is a family, and each member behaves differently.
While circulating nicotinic acid itself has not been studied as a predictive biomarker in large cohort studies, dietary niacin intake (the amount of niacin from food) has been linked to mortality outcomes in several large analyses. These studies measured food intake, not blood levels, so they do not directly validate this test. But they provide biological context for why maintaining adequate niacin supply matters.
In a study of about 26,750 U.S. adults followed for a median of roughly 9 years, those in the highest quarter of dietary niacin intake had about 26% lower risk of death from any cause and 27% lower risk of death from cardiovascular disease compared to those in the lowest quarter, after adjusting for demographics, lifestyle, and health conditions.
Similar patterns appeared in more specific populations. Among roughly 8,750 people with metabolic syndrome (a cluster of conditions including high blood sugar, high blood pressure, and excess abdominal fat), those with the highest dietary niacin intake had about 32% lower all-cause mortality and 37% lower cardiovascular mortality compared to the lowest intake group. Among roughly 4,400 people with established heart disease, the highest intake quarter showed about 26% lower all-cause mortality and 33% lower cardiovascular mortality.
Among about 13,200 people with high blood pressure followed for roughly 8.5 years, the relationship between dietary niacin and mortality was not a simple "more is better" line. Instead, it followed a U-shaped curve: moderate intake was associated with the lowest risk, while both very low and very high intakes were associated with higher risk. The sweet spot appeared to be in the third quarter of intake, where all-cause mortality was about 21% lower than in the lowest quarter.
This pattern suggests that there may be a range of optimal niacin availability rather than a simple threshold. Too little is clearly harmful. But emerging evidence on niacin's breakdown products raises questions about whether too much could also be problematic.
A 2024 study found that two breakdown products of excess niacin (called 2PY and 4PY) were associated with higher rates of major cardiovascular events. People with the highest levels of 4PY had roughly double the cardiovascular risk compared to those with the lowest levels. The proposed mechanism involves these metabolites triggering inflammation in blood vessel walls through a signaling molecule called VCAM-1.
This is an early finding from a single research group, and it applies to niacin metabolites rather than to nicotinic acid itself. But it adds nuance to the picture: the goal is adequate niacin, not maximal niacin. It also helps explain why high-dose niacin supplements (1,000 mg/day and above) failed to prevent heart attacks and strokes in major clinical trials, despite producing favorable changes on standard cholesterol tests.
For decades, doctors prescribed high-dose niacin (1 to 3 grams daily) to improve cholesterol numbers. It worked impressively on paper: HDL cholesterol went up by 20-35%, LDL cholesterol dropped by 10-20%, and triglycerides fell by 20-50%. But when large trials tested whether these improvements translated into fewer heart attacks and strokes, the answer was no.
A Cochrane review pooling 23 randomized trials with about 39,200 participants found no reduction in overall mortality, cardiovascular mortality, heart attacks, or strokes from niacin therapy. A separate analysis of 17 studies with about 35,800 patients confirmed the same null result. Current guidelines from the American Association of Clinical Endocrinology and the American Diabetes Association now recommend against niacin for cardiovascular prevention.
The disconnect between food-sourced niacin (associated with lower mortality) and supplemental niacin (no cardiovascular benefit, increased side effects) is striking. It likely reflects a combination of factors: dietary niacin studies may capture the benefits of overall diet quality rather than niacin alone, and pharmacologic doses of niacin produce side effects (liver toxicity, blood sugar spikes, gout flares) that may cancel out any lipid benefits.
At the extreme low end, severe niacin deficiency causes pellagra, a condition defined by the triad of skin inflammation (especially on sun-exposed areas), diarrhea, and cognitive decline. Left untreated, pellagra can be fatal. In modern Western countries, pellagra is rare but still occurs. The most common causes are alcohol use disorder (accounting for about 35% of cases in published literature), medications that interfere with niacin metabolism such as the tuberculosis drug isoniazid (about 25% of cases), and malabsorption conditions (about 13% of cases).
A rare genetic condition called Hartnup disease, which disrupts the intestinal transport of tryptophan, can also cause pellagra. And research has shown that genetic defects in NAD synthesis pathways can cause birth defects including heart, kidney, spine, and limb abnormalities, which can be prevented by niacin supplementation during pregnancy.
No clinical consensus ranges exist for circulating nicotinic acid levels. This test is a Tier 3, research-level measurement, and standardized interpretation tiers have not been established by any guideline body. What the research does provide is pharmacokinetic data: after a 1-gram oral dose of niacin, peak plasma concentrations typically reach 15 to 30 micrograms per milliliter (a unit for measuring very small concentrations in blood) within 30 to 60 minutes, then drop rapidly due to a very short half-life of 20 to 45 minutes.
For assessing whether your body has enough niacin, the traditional clinical approach uses urinary metabolites rather than blood nicotinic acid levels. Combined measurement of two niacin breakdown products in urine achieved 91% sensitivity and 72% specificity for detecting pellagra. Whole-blood NAD and NADP concentrations failed to detect clinical pellagra in one study, meaning that even people with obvious deficiency symptoms sometimes had normal-looking NAD levels in their blood.
Because no Optimal/Normal/Elevated tiers exist for this specific analyte, the most meaningful way to use this measurement is by tracking your own trend over time within the same lab, rather than comparing a single reading to any published threshold.
A single nicotinic acid reading is a snapshot with limited interpretive power. The molecule clears from your blood in under an hour after absorption, so your level at any given moment is heavily influenced by when you last ate, what you ate, and how quickly your body processed it. This high variability is exactly why serial measurements matter more than any single number.
Get a baseline reading alongside the full NAD profile. If you are making dietary changes, adding or removing supplements, or addressing a condition that affects niacin metabolism, retest in 3 to 6 months using the same lab and the same collection timing. Then retest at least annually. Over time, your personal trend line will be far more informative than any single reading compared to a population average.
This is a newer measurement without standardized cutpoints, but that is exactly why getting a baseline now and tracking your trend gives you a head start. You will have your own data to compare against as the science matures.
Nicotinic acid has an extremely short half-life, which means timing matters more for this test than for most. A blood draw taken 30 minutes after a niacin-rich meal will look very different from one taken several hours later. To get the most consistent readings, draw your blood at the same time of day relative to your last meal each time you test.
Sex also affects levels. Women tend to have higher circulating concentrations of niacin and its breakdown products than men at the same dose, likely due to differences in how quickly the molecule is processed or distributed. If you are comparing your results to a partner's or to published averages, keep this in mind.
Kidney function matters too, since about 88% of a niacin dose is eliminated through the kidneys. Reduced kidney function could slow clearance and produce a falsely elevated reading. And bile acid-binding medications (cholestyramine, colestipol) can bind 10 to 98% of available niacin in the gut, potentially producing a falsely low reading if taken close to your niacin intake.
Evidence-backed interventions that affect your Nicotinic Acid level
Nicotinic Acid is best interpreted alongside these tests.